Two William and Mary students are recipients of summer
research fellowships from the American Physiological Society, continuing the
kinesiology department's excellent record with this competitive award for
undergraduates.

Sarah Todd '10, a kinesiology major, will study the
molecular signaling of blood flow with Robin Looft-Wilson, assistant professor
of kinesiology at William & Mary. Daniel Sinden '11, a neuroscience and
philosophy major, will serve his fellowship at the University of Virginia
School of Medicine.

APS fellowships are awarded to only 24 undergraduates
nationally each year, and William and Mary's kinesiology department has hosted
five APS fellows during the past four years; three in Looft-Wilson's lab and
two working in the lab of Brennan Harris.

Each fellow receives a $4,000 stipend to cover living
expenses during the 10-week fellowship and will present their work at the
society's Experimental Biology 2010 meeting, expected to attract nearly 14,000
scientists.

In Looft-Wilson's lab this summer, Todd will study how
arteries respond to the mechanical effects of blood flow at the molecular
level, work that has important implications for cardiovascular disease and
stroke, which are promoted by disturbed or decreased blood flow.

"Cardiovascular disease is one of the leading causes of
death in the United States. Also, with aging, your blood vessels deteriorate,"
Todd explained. "Professor Looft-Wilson is working with blood vessels and the
signaling mechanism between different layers of cells, when they dilate and
contract. When the blood vessels dilate and contract, it helps with flow."

Sinden will be working on a problem arising after the
repair of blood vessels that have been closed up by the effects of
atherosclerosis, or other cardiovascular diseases.

"A common method of opening them back up again is to use a
wire mesh stent. The problem is that the blood vessels will grow over these
stents, and get closed all over again," he explained. "I'm going to be
researching how certain antiproliferative drugs that are applied to these
stents can stop this overgrowing of the stent through changes in specific gene
expression."